Intrathecal use of amikacin: a case report

Meningitis caused by Acinetobacter baumannii is rare and are mostly hospital acquired after neurosurgical procedure. We report a case of a 40-year old man was admitted to the intensive care unit due to subarachnoid haemorrhage. Our patient developed a ventriculitis due to A.baumannii treated successfully with sulbactam IV and intrathecal amikacin.

Intrathecal use of amikacin: a case report.

Meningitis caused by Acinetobacter baumannii is rare and are mostly hospital acquired after neurosurgical procedure. We report a case of a 40-year old man was admitted to the intensive care unit due to subarachnoid haemorrhage. Our patient developed a ventriculitis due to A.baumannii treated successfully with sulbactam IV and intrathecal amikacin.

[Electrophysiological aspects of intermediate syndrome in organophosphate poisonings]. / Aspects électrophysiologiques du syndrome intermédiaire au cours des intoxications aux organophosphorés.

Acute organophosphate poisoning, whether accidental or suicidal, is frequent in developing countries and produces significant morbidity and mortality. Organophosphates inhibit cholinesterase activity at the neuromuscular junction and cause extensive muscle paralysis, particularly for respiratory function. Poisonings evolve in three stages: cholinesterase crisis, intermediate syndrome and delayed neuropathy. Electrophysiological aspects have been poorly studied. We report the case of a 25-year-old woman admitted to intensive care unit with muscarinic signs and respiratory failure after attempted suicidal organophosphate poisoning. Cholinesterase activity was low and the electrophysiological study disclosed the characteristic aspect of intermediate syndrome. The patient died due to septic complications. This syndrome is exceptional with a poorly understood pathophysiology. The electrophysiological study is essential for diagnosis.

[Clinical and electrophysiological aspects of acute organophosphate intoxication]. / Aspects cliniques et électrophysiologiques de l'intoxication aiguë aux organophosphorés.

INTRODUCTION: Acute organophosphate (OP) intoxications, accidental or voluntary, are responsible for a high mortality. They cause extensive muscular paralysis by acetyl cholinesterase activity inhibition at the neuromuscular junction level. AIM: To underline the rarity and the characteristic electrophysiological pattern during cholinergic crisis. OBSERVATION: A 28-year-old woman was admitted to the medical intensive care unit for Malathion acute intoxication with signs of glandular hypersecretion, complicated tetraparesis, and respiratory distress. The cholinesterase activity was 17%. The electroneuromyography showed multiple motor responses to the same stimulation, which is characteristic of the cholinergic crisis. Other electrophysiological parameters, in particular low-frequency repetitive stimulations, were normal. The evolution was favourable after symptomatic treatment and respiratory assistance. DISCUSSION AND CONCLUSIONS: Organophosphate intoxications evolve in three phases: acute cholinergic crisis, intermediate syndrome, and delayed neuropathy. While the electrophysiological aspects of delayed neuropathy are best characterized, those of crisis and intermediate syndrome remain very little studied. The persistence of acetylcholine in the synaptic slit would explain the multiple motor responses to single stimulation during the crisis.

[Imported severe malaria in adults: a retrospective study of ten cases admitted to intensive care units in Casablanca]. / Paludisme grave d'importation chez l'adulte: étude rétrospective de dix cas admis en réanimation à Casablanca.

INTRODUCTION: We report a retrospective study in the medical intensive care unit of the Casablanca Ibn-Rochd University hospital. MATERIAL AND METHODS: All patients over 14 years of age with falciparum malaria, who were admitted to ICUs between 1996 and 2001, were included. The main epidemiological features, criteria of admission, treatment, and outcome were investigated. RESULTS: Ten patients were included for severe imported malaria. The mean age was 32+/-4 years. All patients had acquired falciparum malaria in sub-Saharan Africa. Chemoprophylaxis was inadequate in all patients. The mean time from symptom onset to treatment initiation was 9+/-2 days. Criteria of admission were impaired consciousness (7), acute renal failure (4), and respiratory distress (3). The most worrying factors were the severity of consciousness disorders, the acute respiratory distress syndrome, the metabolic acidosis, and the refractory shock. All patients presented with nosocomial respiratory infection related to Gram-negative bacilli, in the evolution. All patients received quinine therapy with loading dose and symptomatic treatment. Five patients died. CONCLUSION: The lethality of severe imported malaria is still high despite optimal management in ICUs. Improving chemoprophylaxis and an earlier diagnosis may reduce significantly the mortality rate.

[Rhabdomyolysis and paraphenylene-diamine poisoning]. / Rhabdomyolyse et intoxication à la paraphénylène-diamine.

OBJECTIVE: The aim of this study is to describe clinical description, biological findings, outcome and prognostic factors of paraphenylene-diamine poisoning. PATIENTS AND METHODS: We report a cohort study spreaded over 6 years (1999-2004), realized in Medical Intensive Care Unit in Ibn-Rochd University Hospital at Casablanca (Morocco). This study included 315 patients admitted for paraphenylene-diamine (PPD) poisoning. Diagnosis was based on: poisoning reported by the patient or his family, clinical data, biological findings and qualitative determination of PPD. Epidemiological parameters was obtained at admission. Every day, clinical and biological data, therapy and gravity scores were collected and a mean was calculated. RESULTS: 315 patients were admitted over this period. The mean age was 23+/-9 years. We noticed a clear female predominance (sex-ratio=9.86). The intoxication was voluntarily aiming at autolysis in 93.3% of the cases. The patients were admitted at about 5+/-5.3 hours after the intoxication. The clinical chart was at first dominated by the respiratory and renal symptoms. The mean of CPK was 132,351.8+/-164,978 UI/l. The treatment was especially symptomatic. The mortality was 47%. The multivariate analysis concluded that acid urinary pH, hyperglycaemia, hard muscles, betamimetic drugs and MPM II>0.14 were associated with a poor prognosis. CONCLUSION: The PPD poisoning represents the first cause of toxic rhabdomyolysis in our context and responsible of high mortality. For that, it's necessary to control PPD trade, to inform the medical persons and a rapid management.